scholarly journals Fabrication of Ag nanoparticles mediated by extract of plant and determination of the ‎anti-human lung cancer effects

2021 ◽  
Author(s):  
Hongjiang Yan ◽  
Ruoxuan Xu ◽  
Yanmei Song ◽  
Weinian Gao ◽  
Helin Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Aqueous Extract ◽  
Ag Nanoparticles ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Ag Nps ◽  
Human Lung Adenocarcinoma ◽  
Vis Spectroscopy ◽  
Thymus Capitatus

IntroductionThe present work demonstrates the synthesis of Ag nanoparticles (Ag NPs) by aqueous extract of Thymus ‎capitatus as green reductant and capping agent without any toxic reagent. ‎Material and methodsPhysicochemical characteristics of the said nanocomposite were elucidated by field emission scanning electron ‎microscopy (FE-SEM), fourier-transform infrared spectroscopy (FTIR), and UV-Vis Spectroscopy. ‎ResultsThe biogenic Ag NPs are uniformly globular. The Ag NPs has been explored biologically in the anticancer and ‎antioxidant assays. In the cellular and molecular part of the recent study, the treated cells with Ag NPs were ‎assessed by MTT assay for 48h about the cytotoxicity and anti-human lung adenocarcinoma properties on ‎normal (HUVEC) and lung adenocarcinoma cell lines i.e. lung well-differentiated bronchogenic adenocarcinoma ‎‎(HLC-1), lung moderately differentiated adenocarcinoma (LC-2/ad), and lung poorly differentiated ‎adenocarcinoma (PC-14). The viability of malignant lung cell line reduced dose-dependently in the presence of ‎Ag NPs. The IC50 of Ag NPs were 209, 185, and 106 µg/mL against HLC-1, LC-2/ad, and PC-14 cell lines, ‎respectively. In the antioxidant test, the IC50 of Ag NPs and BHT against DPPH free radicals were 86 and 76 ‎‎µg/mL, respectively. ‎ConclusionsAfter clinical study, Ag NPs containing Thymus capitatus leaf aqueous extract may be used to formulate a new ‎chemotherapeutic drug or supplement to treat the several types of human lung adenocarcinoma. ‎

scholarly journals Novel Curcumae Kwangsiensis mediated synthesis of silver nanoparticles for anti-lung cancer activity: a preclinical trial study

2021 ◽  
Author(s):  
Zhihong Liu ◽  
Zhuohong Zhang ◽  
Xiaomei Du ◽  
Ying Liu ◽  
Abdullah Alarfaj ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Silver Nanoparticles ◽  
Cell Lines ◽  
Cancer Cell ◽  
Aqueous Extract ◽  
Ag Nanoparticles ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Leaf Aqueous Extract

IntroductionThe present work indicated the green synthesis and characterization and cytotoxicity, antioxidant, and anti-human lung cancer activities of silver nanoparticles containing Curcumae Kwangsiensis Folium leaf aqueous extract.Material and methodsAg nanoparticles have been produced by mixing the AgNO3 solution with aqueous Curcumae Kwangsiensis Folium leaf extract. Characterization of Ag nanoparticles was done by FE‐SEM, FT‐IR, TEM, and UV-Vis. FE-SEM and TEM images revealed an average diameter of 15-21 nm for the nanoparticles. MTT assay was used on common human lung cancer cell lines i.e., lung well-differentiated bronchogenic adenocarcinoma (HLC-1), lung moderately differentiated adenocarcinoma (LC-2/ad), and lung poorly differentiated adenocarcinoma (PC-14) cell lines to survey the cytotoxicity and anti-human lung cancer effects of Ag nanoparticles.ResultsThey had very low cell viability and high anti-human lung cancer activities dose-dependently against HLC-1, LC-2/ad, and PC-14 cell lines without any cytotoxicity on the normal cell line (HUVEC). The IC50 of Ag nanoparticles were 249, 187, and 152 µg/mL against HLC-1, LC-2/ad, and PC-14 cell lines, respectively. The best results of cytotoxicity and anti-human lung cancer properties were seen in the concentration of 1000 µg/mL. Ag nanoparticles inhibited half of the DPPH molecules in the concentration of 135 µg/mL.ConclusionsMaybe significant anti-human lung cancer potentials of Ag nanoparticles synthesized by Curcumae Kwangsiensis Folium leaf aqueous extract against common human lung cancer cell lines are linked to their antioxidant activities. After confirming the above results in the clinical trial researches, this formulation can be administrated to treat human lung cancers in humans.

The ADAM17 protease promotes tobacco smoke carcinogen-induced lung tumorigenesis

2019 ◽  
Vol 41 (4) ◽  
pp. 527-538 ◽  
Author(s):  
Mohamed I Saad ◽  
Louise McLeod ◽  
Liang Yu ◽  
Hiromichi Ebi ◽  
Saleela Ruwanpura ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Tobacco Smoke ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Smoking History ◽  
Lung Carcinogenesis ◽  
Wild Type Littermate ◽  
Human Lung Adenocarcinoma ◽  
Erk Mapk

Abstract Lung cancer is the leading cause of cancer-related mortality, with most cases attributed to tobacco smoking, in which nicotine-derived nitrosamine ketone (NNK) is the most potent lung carcinogen. The ADAM17 protease is responsible for the ectodomain shedding of many pro-tumorigenic cytokines, growth factors and receptors, and therefore is an attractive target in cancer. However, the role of ADAM17 in promoting tobacco smoke carcinogen-induced lung carcinogenesis is unknown. The hypomorphic Adam17ex/ex mice—characterized by reduced global ADAM17 expression—were backcrossed onto the NNK-sensitive pseudo-A/J background. CRISPR-driven and inhibitor-based (GW280264X, and ADAM17 prodomain) ADAM17 targeting was employed in the human lung adenocarcinoma cell lines A549 and NCI-H23. Human lung cancer biopsies were also used for analyses. The Adam17ex/ex mice displayed marked protection against NNK-induced lung adenocarcinoma. Specifically, the number and size of lung lesions in NNK-treated pseudo-A/J Adam17ex/ex mice were significantly reduced compared with wild-type littermate controls. This was associated with lower proliferative index throughout the lung epithelium. ADAM17 targeting in A549 and NCI-H23 cells led to reduced proliferative and colony-forming capacities. Notably, among select ADAM17 substrates, ADAM17 deficiency abrogated shedding of the soluble IL-6 receptor (sIL-6R), which coincided with the blockade of sIL-6R-mediated trans-signaling via ERK MAPK cascade. Furthermore, NNK upregulated phosphorylation of p38 MAPK, whose pharmacological inhibition suppressed ADAM17 threonine phosphorylation. Importantly, ADAM17 threonine phosphorylation was significantly upregulated in human lung adenocarcinoma with smoking history compared with their cancer-free controls. Our study identifies the ADAM17/sIL-6R/ERK MAPK axis as a candidate therapeutic strategy against tobacco smoke-associated lung carcinogenesis.

scholarly journals An Investigation on Cytotoxicity Effect of Putrescine-Sulphur Analogues on Breast Cancer (Mcf-7), Human Lung Adenocarcinoma (A549) and Colorectal Cancer (Hct-8) Cell Lines

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Norsuhana Halim ◽  
Radiah Abdul Ghani ◽  
Adzly Hairee Sahabudin ◽  
Fiona How Ni Fong
Keyword(s):  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Cell Lines ◽  
Human Lung ◽  
Breast Adenocarcinoma ◽  
Normal Cells ◽  
Human Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Specific Cancer ◽  
Mcf 7

Introduction: Cancer is one of the global health problems that has a detrimental effect to a person's life. However, chemotherapeutic agents success are subject to the side effects due to lack of specificity in the drug delivery system to cancer cells and an increase risk of systemic toxicity to the normal cells. Polyamine transport system (PTS) is one of the potential pathways for transporting anticancer agent into specific cancer cells. This is due to the upregulation of PTS in cancer cells compared to normal cells for the proliferation activity. The aim of this study was to investigate the cytotoxicity effect of putrescine-sulphur analogues type 1 (PSA-1) and type 2 (PSA-2) on human lung adenocarcinoma cells (A549), human colorectal adenocarcinoma cells (HCT-8) and human breast adenocarcinoma cell (MCF-7). Materials and method: The cytotoxicity effect of newly synthesized PSA-1 and PSA-2 were evaluated on selected cancer cells; MCF-7, A549 and HCT-8 cell lines. The halfmaximal inhibitory concentration (IC50) obtained from tetrazolium bromide (MTT) assay was derived from the dose-response graph for all cell lines. Results: PSA-2 elicited cytotoxicity effect, eventhough the IC50 values were not potent with IC50 of 5.4 mM, 5.2 mM and 7.0 mM for MCF-7/48h, A549/48h and HCT-8/48h, respectively. The PSA-1 compound exhibited cytotoxicity effect in all cell lines, however, the compound failed to induce anti-proliferation at the concentration of 3 mM and above. The cytotoxicity of PSA-2 compound against MCF-7 cell lines showed higher potency compared to A549 and HCT-8 cell lines. Conclusion: It was suggested that PSA-2 compound was able to exert cytotoxicity effect against selected cancer cells, in low potency and is deemed for further investigation to increase its effectiveness against specific cancer cells.

scholarly journals Transcriptional Response of Ovine Lung to Infection with Jaagsiekte Sheep Retrovirus

2019 ◽  
Vol 93 (21) ◽  
Author(s):  
Anna Eleonora Karagianni ◽  
Deepali Vasoya ◽  
Jeanie Finlayson ◽  
Henny M. Martineau ◽  
Ann R. Wood ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Animal Model ◽  
Lung Adenocarcinoma ◽  
Human Lung ◽  
Transcriptional Response ◽  
Human Lung Cancer ◽  
Ovine Pulmonary Adenocarcinoma ◽  
Jaagsiekte Sheep Retrovirus ◽  
Human Lung Adenocarcinoma ◽  
Naturally Occurring

ABSTRACT Jaagsiekte sheep retrovirus (JSRV) is the etiologic agent of ovine pulmonary adenocarcinoma (OPA), a neoplastic lung disease of sheep. OPA is an important economic and welfare issue for sheep farmers and a valuable naturally occurring animal model for human lung adenocarcinoma. Here, we used RNA sequencing to study the transcriptional response of ovine lung tissue to infection by JSRV. We identified 1,971 ovine genes differentially expressed in JSRV-infected lung compared to noninfected lung, including many genes with roles in carcinogenesis and immunomodulation. The differential expression of selected genes was confirmed using immunohistochemistry and reverse transcription-quantitative PCR. A key finding was the activation of anterior gradient 2, yes-associated protein 1, and amphiregulin in OPA tumor cells, indicating a role for this oncogenic pathway in OPA. In addition, there was differential expression of genes related to innate immunity, including genes encoding cytokines, chemokines, and complement system proteins. In contrast, there was little evidence for the upregulation of genes involved in T-cell immunity. Many genes related to macrophage function were also differentially expressed, reflecting the increased abundance of these cells in OPA-affected lung tissue. Comparison of the genes differentially regulated in OPA with the transcriptional changes occurring in human lung cancer revealed important similarities and differences between OPA and human lung adenocarcinoma. This study provides valuable new information on the pathogenesis of OPA and strengthens the use of this naturally occurring animal model for human lung adenocarcinoma. IMPORTANCE Ovine pulmonary adenocarcinoma is a chronic respiratory disease of sheep caused by jaagsiekte sheep retrovirus (JSRV). OPA is a significant economic problem for sheep farmers in many countries and is a valuable animal model for some forms of human lung cancer. Here, we examined the changes in host gene expression that occur in the lung in response to JSRV infection. We identified a large number of genes with altered expression in infected lung, including factors with roles in cancer and immune system function. We also compared the data from OPA to previously published data from human lung adenocarcinoma and found a large degree of overlap in the genes that were dysregulated. The results of this study provide exciting new avenues for future studies of OPA and may have comparative relevance for understanding human lung cancer.

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